Circ_0132817 facilitates cell proliferation, migration, invasion and glycolysis by regulating the miR-432-5p/NOL4L axis in neuroblastoma

Fang, Yafei; Yao, Yuqian; Mao, Kangwei; Zhong, Yanyan; Xu, Yan

doi:10.1007/s00221-021-06091-y

Cited by 10 publications

(7 citation statements)

References 31 publications

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“…knockdown may lead to the tumorigenesis of neuroblastoma, a sympathetic nervous system malignancy (Fang et al, 2021). such as the intestinal microbiome (Voigt et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Using human genetics to understand the phenotypic association between chronotype and breast cancer

Yang

Zou

et al. 2023

Journal of Sleep Research

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SummaryLittle is known regarding the shared genetic influences underlying the observed phenotypic association between chronotype and breast cancer in women. Leveraging summary statistics from the hitherto largest genome‐wide association study conducted in each trait, we investigated the genetic correlation, pleiotropic loci, and causal relationship of chronotype with overall breast cancer, and with its subtypes defined by the status of oestrogen receptor. We identified a negative genomic correlation between chronotype and overall breast cancer ( = −0.06, p = 3.00 × 10−4), consistent across oestrogen receptor‐positive ( = −0.05, p = 3.30 × 10−3) and oestrogen receptor‐negative subtypes ( = −0.05, p = 1.11 × 10−2). Five specific genomic regions were further identified as contributing a significant local genetic correlation. Cross‐trait meta‐analysis identified 78 loci shared between chronotype and breast cancer, of which 23 were novel. Transcriptome‐wide association study revealed 13 shared genes, targeting tissues of the nervous, cardiovascular, digestive, and exocrine/endocrine systems. Mendelian randomisation demonstrated a significantly reduced risk of overall breast cancer (odds ratio 0.89, 95% confidence interval 0.83–0.94; p = 1.30 × 10−4) for genetically predicted morning chronotype. No reverse causality was found. Our work demonstrates an intrinsic link underlying chronotype and breast cancer, which may provide clues to inform management of sleep habits to improve female health.

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“…knockdown may lead to the tumorigenesis of neuroblastoma, a sympathetic nervous system malignancy (Fang et al, 2021). such as the intestinal microbiome (Voigt et al, 2019).…”

Section: Discussionmentioning

confidence: 99%

Using human genetics to understand the phenotypic association between chronotype and breast cancer

Yang

Zou

et al. 2023

Journal of Sleep Research

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“…Circular RNAs might also be considered as regulators of translation [53][54][55][56]. CircRNA-TBC1D4, circRNA-NAALAD2, and circRNA-TGFBR3 may be tumor suppressor genes in neuroblastoma.…”

Section: Discussionmentioning

confidence: 99%

“…If downregulated simultaneously, they may serve as biomarkers of unfavorable neuroblastoma [53]. Other circular RNAs might act as oncogenes: circ_0132817 facilitates cell proliferation, migration, invasion, and glycolysis in neuroblastoma [54]; circPDE5A is upregulated in neuroblastoma tissues and cells and its silencing suppresses neuroblastoma cell proliferation, migration, invasion, and glycolysis in vitro and reduces tumor growth in vivo [55]; circular RNAs with oncogenic properties might even result from MYCN amplification in neuroblastoma cells [56].…”

Section: Discussionmentioning

confidence: 99%

In Vitro Assessment of the Role of p53 on Chemotherapy Treatments in Neuroblastoma Cell Lines

et al. 2021

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Neuroblastoma is the most frequent malignant extracranial solid tumor of infancy. The overall objective of this work consists of determining the presence of alterations in the p53/MDM2/p14ARF signaling pathway in neuroblastoma cell lines and deciphering their possible relationship with resistance to known antineoplastic drugs and to differentiation agents. Firstly, we characterized 10 neuroblastoma cell lines for alterations at the p53/MDM2/p14ARF signaling pathway by analysis of TP53 point mutations, MYCN and MDM2 amplification, and p14ARF methylation, homozygous deletions, and expression. Secondly, we chose SK-N-FI (mutated at TP53) and SK-N-Be(2) (wild-type TP53) cell lines, treated them with chemotherapeutic agents (doxorubicin, etoposide, cisplatin, and melphalan) and with two isomers of retinoic acid (RA): (9-cis and all-trans). Finally, we analyzed the distribution of the cell cycle, the induction of apoptosis, and the expression levels of p53, p21, and Bcl-2 in those two cell lines. P14ARF did not present promoter methylation, homozygous deletions, and protein expression in any of the 10 neuroblastoma cell lines. One TP53 point mutation was detected in the SK-N-FI cell line. MYCN amplification was frequent, while most cell lines did not present MDM2 amplification. Treatment of SK-N-FI and SK-N-Be(2) cells with doxorubicin, etoposide, cisplatin, and melphalan increased apoptosis and blocked the cycle in G2/M, while retinoic acid isomers induced apoptosis and decreased the percentage of cells in S phase in TP53 mutated SK-N-FI cells, but not in TP53 wild-type SK-N-Be(2) cells. Treatment with cisplatin, melphalan, or 9-cis RA decreased p53 expression levels in SK-N-FI cells but not in SK-N-Be (2). The expression of p21 was not modified in either of the two cell lines. Bcl-2 levels were reduced only in SK-N-FI cells after treatment with cisplatin. However, treatments with doxorubicin, etoposide, or 9-cis-RA did not modify the levels of this protein in either of the two cell lines. In conclusion, TP53 mutated SK-N-FI cells respond better to the retinoic isomers than TP53 wild-type SK-N-Be(2) cells. Although these are in vitro results, it seems that deciphering the molecular alterations of the p53/MDM2/p14ARF signaling pathway prior to treating patients of neuroblastoma might be useful for standardizing therapies with the aim of improving survival.

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“…In a similar mechanism of action, Fang et al. found that circCUX1 works through the miR432-5p/NOL4L axis ( 16 ), and Wang found that circCUX1 works through the miR-338-3p/PHF20 axis ( 17 ).…”

Section: Carcinogenic Circrnasmentioning

confidence: 97%

Recent advances and application value of circRNA in neuroblastoma

Tan

Yang

2023

Front. Oncol.

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Neuroblastoma (NB) is children’s most prevalent solid malignant tumor, accounting for 15% of childhood cancer mortality. Non-coding RNA is important in NB pathogenesis. As a newly identified non-coding RNA, abnormal regulation (abnormal up-regulation or down-regulation) of the circRNAs expression is implicated in the tumorigenesis of various tumors, including NB. CircRNAs primarily regulate the expression of microRNA (miRNA) target genes by microRNA (miRNA) sponge adsorption. Clinical evidence suggests that the expression of certain circRNAs is associated with the prognosis and clinical features of NB and hence may be exploited as a biomarker or therapeutic target. This review examines circRNAs that have been demonstrated to play a function in NB.

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Circ_0132817 facilitates cell proliferation, migration, invasion and glycolysis by regulating the miR-432-5p/NOL4L axis in neuroblastoma

Cited by 10 publications

References 31 publications

Using human genetics to understand the phenotypic association between chronotype and breast cancer

Using human genetics to understand the phenotypic association between chronotype and breast cancer

In Vitro Assessment of the Role of p53 on Chemotherapy Treatments in Neuroblastoma Cell Lines

Recent advances and application value of circRNA in neuroblastoma

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